A cerebral haemorrhage (also spelled hemorrhage; also known as a cerebral hematoma) is a type of intracranial hemorrhage (intracranial hematoma) that occurs within the brain tissue itself. It is alternatively called intracerebral hemorrhage. It can be caused by brain trauma, or it can occur spontaneously in hemorrhagic stroke. Non-traumatic intracerebral hemorrhage is a spontaneous bleeding into the brain tissue. Non-traumatic can refer to increased excertion, tension or stress.[1]

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Patients with intraparenchymal bleeds have symptoms that correspond to the functions controlled by the area of the brain that is damaged by the bleed.[3] Other symptoms include those that indicate a rise in intracranial pressure caused by a large mass putting pressure on the brain.[3] Intracerebral hemorrhages are often misdiagnosed as subarachnoid hemorrhages due to the similarity in symptoms and signs. A severe headache followed by vomiting is one of the more common symptoms of intracerebral hemorrhage. Some patients may also go into a coma before the bleed is noticed.

Tramautic intracerebral hematomas are divided into acute and delayed. Acute intracerebral hematomas occur at the time of the injury while delayed intracerebral hematomas have been reported from as early as 6 hours post injury to as long as several weeks.

Both computed tomography angiography (CTA) and magnetic resonance angiography (MRA) have been proved to be effective in diagnosing intracranial vascular malformations after ICH.[10] So frequently, a CT angiogram will be performed in order to exclude a secondary cause of hemorrhage[11] or to detect a "spot sign".

Intraparenchymal hemorrhage can be recognized on CT scans because blood appears brighter than other tissue and is separated from the inner table of the skull by brain tissue. The tissue surrounding a bleed is often less dense than the rest of the brain because of edema, and therefore shows up darker on the CT scan.[11]

Antihypertensive therapy to bring down the blood pressure in acute phases appears to improve outcomes.[12] The AHA/ASA and EUSI guidelines (American Heart Association/American Stroke Association guidelines, and the European Stroke Initiative guidelines) have recommended antihypertensive therapy to stabilize the mean arterial pressure at 110 mmHg.

Giving Factor VIIa within 4 hours limits the bleeding and formation of a hematoma. However, it also increases the risk of thromboembolism.[13] It thus overall does not result in better outcomes in those without hemophilia.[14]

The risk of death from an intraparenchymal bleed in traumatic brain injury is especially high when the injury occurs in the brain stem.[2] Intraparenchymal bleeds within the medulla oblongata are almost always fatal, because they cause damage to cranial nerve X, the vagus nerve, which plays an important role in blood circulation and breathing.[5] This kind of hemorrhage can also occur in the cortex or subcortical areas, usually in the frontal or temporal lobes when due to head injury, and sometimes in the cerebellum.[5][18]

For spontaneous ICH seen on CT scan, the death rate (mortality) is 34–50% by 30 days after the insult,[1] and half of the deaths occur in the first 2 days.[19] Even though the majority of deaths occurs in the first days after ICH, survivors have a long term excess mortality of 27% compared to the general population.[20]

The inflammatory response triggered by stroke has been viewed as harmful in the early stage, focusing on blood-borne leukocytes, neutrophils and macrophages, and resident microglia and astrocytes.[21] A human postmortem study shows that inflammation occurs early and persists for several days after ICH.[22] New area of interest are the Mast Cells.[23]

On April 2, 1951, Russian-born American pianist Simon Barere collapsed and later died from cerebral hemorrhage while playing the first few bars of Edvard Grieg's Piano Concerto in A minor at a performance at Carnegie Hall in New York. [26]

In 1985, television game show announcer Johnny Olson died from a cerebral hemorrhage.